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Medicine > Step Up to Medicine > Flashcards

Step Up to Medicine Flashcards

1
Q

3 most common causes of PUD

A
  1. H Pylori
  2. NSAID
  3. acid hyper secretion (ZES)
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2
Q

pathogenesis of duodenal ulcer: caused by ________

A

increase in offensive factors

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3
Q

pathogenesis of gastric ulcer: caused by ________

A

decrease in defensive factors

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4
Q

H Pylori infection more common in _________ ulcers

A

duodenal

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5
Q

4 types of gastric ulcers

A

type I: lesser curvature
type II: gastric and duodenal ulcer
type III: prepyloric
type IV: near GE junction

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6
Q

dx and tx for uncomplicated PUD

A

initiate empiric therapy

no need for Ba or endoscopy

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7
Q

how to work up gastric ulcer

A

must do endoscopy and biopsy to r/o cancer

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8
Q

how to dx h pylori

A

gold standard: endoscopic biopsy
urea breath test- acute infection
serology (lower specificity)- positive for life

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9
Q

initial and recurrent H pylori therapy

A

initial: triple therapy (PPI, amoxicillin, clarithromycin)
recurrent: quadruple therapy (PPI, bismuth, 2 abx)

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10
Q

cytoprotection drugs for PUD

A

sucralfate and misoprostol

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11
Q

how to tx NSAID induced ulcer

A

stop NSAID

start PPI or misoprostol for 4-8 weeks

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12
Q

when to discontinue PPI after PUD

A

after 4-6 weeks in patient with uncomplicated ulcers who are asymptomatic

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13
Q

how to tx PUD that’s NOT related to H Pylori or NSAID use

A

PPI

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14
Q

most common cause of upper GI bleeding

A

PUD

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15
Q

when to do surgery in PUD

A

to tx complications: perforation, GOO, bleeding

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16
Q

common causes of acute gastritis

A

NSAID, H Pylori, alcohol, heavy cigarette smoking

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17
Q

how to tx acute gastritis

A
  • if pain low/mod and no worrisome sxs –> PPI, stop NSAID

- if no response in 4-8 weeks, then do upper GI endoscopy and ultrasound and test for h pylori

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18
Q

most common cause of chronic gastritis

A

h pylori

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19
Q

auto-immune gastritis leads to chronic atrophic gastritis with ________ antibodies

A

serum antiparietal and anti-intrinsic factor –> pernicious anemia

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20
Q

how to dx and tx chronic gastritis

A

dx with upper GI endoscopy with biopsy

tx symptomatic pt with H. Pylori eradication

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21
Q

most gastric cancers are _________ (type of morphology)

A

adenocarcinoma

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22
Q

risk factors for gastric adenocarcinoma

A

gastritis, adenomatous gastric polyps, h pylori, pernicious anemia, post-antrectomy, menetrier’s disease

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23
Q

dx of gastric cancer

A

EGD with multiple biopsies, Ba upper GI studies (if needed), abdominal CT for staging, FOBT

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24
Q

tx gastric cancer

A 
wide excision (total or subtotal gastrectomy) with LN dissection
\+/- chemo
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25
Q

pt with chronic stable angina presents with sxs of USA… 3 initial steps?

A
  1. ECG and cardiac enzymes
  2. aspirin
  3. IV heparin
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26
Q

tests to order for a new pt with CHF

A 
CXR
ECG (r/o MI)
cardiac enzymes 
CBC (r/o anemia)
echo
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27
Q

what do you often see on CXR of heart failure?

A

cardiomegaly
interstitial markings
pleural effusion
kerley B lines (horizontal lines near the costophrenic angle)

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28
Q

initial test of choice in heart failure

A

transthoracic echo

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29
Q

cut off for preserved EF and reduced EF

A

40%

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30
Q

most precise test for assessing LV function and EF…

A 
nuclear ventriculography (radionuclide ventriculography using technetium 99m)
mostly not ordered...
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31
Q

treatments for systolic dysfunction heart failure

A 
lifestyle modification
diurectis
spironolactone
ACEI/ARBs
beta-blockers
digitalis 
hydralazine and isosorbide dinitrates 
ICD and CRT
cardiac transplant
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32
Q

most effective symptomatic relief drug for heart failure

no benefit for mortality

A

diuretics

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33
Q

spironolactone in heart failure

when to avoid?

A

prolongs survival in select patients (classes III and IV)

avoid in renal failure pts

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34
Q

initial treatment in most symptomatic heart failure patients

A

diuretic and ACEI

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35
Q

ACEI in CHF

A

prolongs survival and alleviates sxs in all classes of CHF

all pts with systolic dysfunction should be on an ACEI even if they have no sxs

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36
Q

beta blockers in heart failure

A

decreases mortality in pts with post-MI heart failure
give only to STABLE pts with class I-III heart failure
carvedilol > metoprolol

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37
Q

digitalis in heart failure

A

no mortality benefit

for pts with sxs despite optimal therapy (with ACEI, beta blocker, aldo antag, and diuretic)

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38
Q

hydrazine and isosorbide dinitrates

A

used in pts who can’t take ACEI

-improves mortality but just not as good as ACEI

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39
Q

standard CHF treatment based on severity of disease

A

mild: diuretic and ACEI
mod: add beta blocker
severe: add digoxin and then spironolactone

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40
Q

most common cause of death from CHF

A

sudden death from ventricular arrhythmias (2/2 ischemia)

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41
Q

meds that lower mortality in CHF

A

beta blockers
ACEI and ARBs
aldo antags (spironolactone)
hydralazine/nitrates

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42
Q

nausea/vomiting, anorexia, ectopic ventricular beats, AV block, a fib, visual disturbances, disorientation
pt with heart failure

A

signs of digoxin toxicity

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43
Q

CCB in CHF

A

no role/not indicated

felodipine and amlodipine are safe if needed for another condition

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44
Q

what MUST you do if someone is on a VAD (ventricular assist device)

A

lifelong anticoagulation with heparin or warfarin

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45
Q

meds contra-indicated in CHF patients

A

metformin- lactic acidosis
thiazolidinediones- fluid retention
NSAIDs- exacerbation
antiarrhythmic agents w/ negative inotropic effects

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46
Q

2 devices that reduce mortality in CHF patients

A 
ICD and CRT (long QRS) 
EF < 35%, class II or III with sxs despite meds
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47
Q

how to tx diastolic dysfunction

A

beta blockers
diuretics
NO digoxin and spironolactone
MAYBE ACEI/ARBs

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48
Q

Treatment of acute decompensating heart failure

A

O2
Diuretics
Nitrates if not hypotensive
+/- dobutamine (digoxin takes a few weeks to take effect)

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49
Q

2 classic types of COPD

A

chronic bronchitis

emphysema

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50
Q

chronic bronchitis is a _______ dx

what are the criteria

A

clinical

chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years

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51
Q

emphysema is a ______ dx

what are the criteria

A

pathologic

permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls

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52
Q

COPD is the ______ leading cause of death in the US

A

4th

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53
Q

what type of emphysema is this?
smokers
destruction of only respiratory (proximal) bronchioles
upper lung zones

A

centrilobular

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54
Q

what type of emphysema is this?
alpha-1-antitrypsin deficiency
destruction of both proximal and distal acini
lung bases

A

panlobular

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55
Q

emphysema results due to too much _________ and not enough _______

A

too much protease (elastase)

not enough antiprotease (alpha1-antitrypsin)

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56
Q

cough, sputum production, dyspnea in a smoker

most likely dx?

A

COPD

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57
Q

most common early sxs of COPD

A

exertional dyspnea

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58
Q

in COPD,
FEV1 is _____
TLC is _____
RV is _______

A

decreased
increased
increased

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59
Q 
thin
lean forward
barrel chest
tachypnea
respiratory distress and accessory muscle use
A

pink puffer (emphysema)

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60
Q 
overweight and cyanotic
chronic cough
sputum production
cor pulmonale 
respiratory rate normal
no apparent distress
A

blue boaters (predominant chronic bronchitis)

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61
Q

signs of COPD

A

prolonged forced expiratory time
end expiratory wheeze
decrease breath sound
inspiratory crackle

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62
Q

to dx airway obstruction, one must have a normal or increased ______ with decreased ________

A

TLC

FEV1

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63
Q

definitive dx test for COPD

A

PFTs (spirometry)

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64
Q

obstruction on PFT is evidenced by _______ and ________

A

decreased FEV1
< 50% severe
50-70% moderate
decreased FEV1/FVC ratio

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65
Q 
obstructive pattern lung volumes
TLC
residual volume
FRC
VC
A

increased
increased
increased
decreased

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66
Q

CXR as a dx for COPD?

A

not very sensitive but will show:
hyperinflation
flattened diaphragm
enlarged retrosternal space

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67
Q

good screening tool for obstructive dz

A

if peak flow meter shows < 350 L/min –> get PFT

this is a good triage method, esp in the ED

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68
Q

in patients with personal or FH of emphysema before age 50, do this

A

measure alpha1-antitrypsin

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69
Q

COPD ABG

A

hypoxemia
hypercapnea
respiratory acidosis with metabolic alkalosis compensation

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70
Q

most important intervention in COPD

A

stop smoking

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71
Q

best way to clinically monitor COPD pts

A

serial FEV1 measurements

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72
Q

interventions shown to improve mortality in COPD

A

smoking cessation

home O2

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73
Q

_________ are contraindicated in acute COPD or asthma exacerbation

A

beta blockers

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74
Q

mechanism of COPD causing cor pulmonale

A

COPD –> hypoxemia –> hypoxic vasoconstriction –> pulmonary HTN –> cor pulmonale

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75
Q

vaccines for COPDers

A

annual flu

strep pneumo q5-6 years

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76
Q

_____________ are only used for acute COPD exacerbations and should not be used for long term treatment

A

IV glucocorticoids

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77
Q

home O2 therapy criteria for COPDers

A

any of the following:
PaO2 55
O2 sat < 88% rest or exercise
PaO2 55-49 plus evidence of polycythemia or cor pulmonale

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78
Q

theophylline mechanism of action

A

improve mucociliary clearance and central respiratory drive

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79
Q

mild to moderate COPD tx

A
  • first line: bronchodilator (combo of beta agonist and anticholinergic is the most effective)
  • inhaled glucocorticoids may be used
  • consider theophylline for refractory cases
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80
Q

severe COPD tx

A
  • first line: inhaler with bronchodilator (combo of beta agonist and anticholinergic is the most effective)
  • inhaled glucocorticoids may be used
  • consider theophylline for refractory cases

+

O2, pulm rehab, triple inhaler therapy (LABA, long acting anticholinergic, inhaled glucocorticoid)

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81
Q

COPD exacerbation tx

A
  • CXR
  • beta agonist +/- anticholinergic
  • IV glucocorticoids for pts in the hospital
    • don’t use inhaled glucocorticoids in exacerbation
  • abx (azithromycin, levofloxacin)
  • supp O2
  • BIPAP or CPAP
  • intubation and mechanical ventilation if needed
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82
Q

3 complications of COPD

A

acute exacerbations (noncompliance, infection, cardiac dz)
secondary polycythemia
pulmonary HTN and cor pulmonale

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83
Q

chronic tx of asthma

mild intermittent

A

2 or fewer times/week

no meds

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84
Q

chronic tx of asthma

mild persistent

A

2 or more times/week but not every day

low dose inhaled corticosteroid

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85
Q

chronic tx of asthma

moderate persistent

A

daily sxs, frequent exacerbations

  • daily inhaled CS (low dose) or
  • cromolyn/nedocromil (prophylaxis b4 exercise in kids) or
  • methylxanthine or
  • antileukotriene (ex. montelukast)
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86
Q

chronic tx of asthma

severe persistent

A

continual sxs, frequent exacerbations, limited physical activity

  • daily inhaled CS (high dose) and LABA or
  • methylxanthine and systemic CS
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87
Q

triad of asthma

A

airway inflammation
airway hyper-responsiveness
reversible airflow obstruction

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88
Q

asthma is only present in young children (t/f)

A

F

it can begin at any age

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89
Q

extrinsic vs intrinsic asthma

which is more common

A

extrinsic- pts are atopic and become asthmatic at a young age

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90
Q

SOB, wheezing, chest tightness, cough, worse at night

most likely dx

A

asthma

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91
Q

ddx of wheezing

A 
asthma
CHF
COPD
cardiomyopathies
lung cancer
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92
Q

most common PE finding in asthma

A

wheezing

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93
Q
  • _______ are required for asthma dx, which show __________
  • in order to be considered reversible airflow obstruction, FEV1 or FVC must increase by at least ____% after bronchodilator administration
A

PFTs, obstructive pattern

12%

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94
Q

what’s the bronchoprovocation test

A

useful for diagnosing asthma when PFTs are nondiagnostic
-measures lung function before and after inhalation of increasing doses of methacholine; hyperresponsive airways develop obstruction at lower doses

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95
Q

CXR in asthma

A

r/o other conditions

asthma doesn’t really show up very well on CXR

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96
Q

ABG interpretation in acute asthma attack

A
  • low CO2 and low O2

- increased CO2 is a sign of respiratory muscle fatigue or severe airway obstruction

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97
Q

what to give for acute asthma attacks

A

SABA (short acting beta agonists)

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98
Q

avoid _______ in asthmatics

A

beta blockers

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99
Q

LABA are particularly good for ________ and __________

A

night time asthma and exercise induced asthma

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100
Q

______ is the quickest method of dxing asthma

A

peak flow measurement

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101
Q

how to manage severe acute asthma exacerbation (hospital admission)

A
  • inhaled beta agonist is first line
  • IV CS –> taper when clinical improvement occurs
  • IV Mg is third line
  • O2- keep sat above 90%
  • abx if severe of you suspect infection
  • intubation if you suspect respiratory failure/impending respiratory failure
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102
Q

side effects of inhaled CS

A

sore throat
thrush
hoarseness

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103
Q

tests to order for acute asthma exacerbation (3)

A

PEF- decreased
ABG- increased A-a gradient
CXR- r/o pneumonia, ptx

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104
Q

3 complications of asthma

A

status asthmaticus- no response to standard meds
acute respiratory failure- respiratory muscle fatigue
ptx, atelectasis, pneumomediastinum

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105
Q

asthma pts with nasal polyps… what are you thinking?

A

aspirin sensitive asthma

do not give aspirin or any NSAID

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106
Q

permanent abnormal dilation and destruction of bronchial walls, cilia are damaged

A

bronchiectasis

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107
Q

2 major causes of bronchiectasis

A

CF

infection

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108
Q

infection in a pt with airway obstruction or impaired defense/drainage precipitates __________

A

bronchiectasis

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109
Q

clinical features of bronchiectasis (4)

A

chronic cough with foul mucopurulent sputum
dyspnea
hemoptysis
recurrent/persistent pneumonia

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110
Q

how to dx bronchiectasis

A

high resolution CT is the best

PFTs show obstructive pattern

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111
Q

how to tx bronchiectasis exacerbation

A

abx

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112
Q

how to tx bronchiectasis on a day to day basis

A

hydration
chest PT
inhaled bronchodilators

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113
Q

goal in the tx of bronchiectasis

A

prevent pneumonia and hemoptysis complications

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114
Q

defect in cystic fibrosis

A

defect in Cl channel –> impaired Cl and water transport –> thick secretions in respiratory tract, exocrine pancreas, sweat glands, intestines, and GU tract

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115
Q

CF shows a (obstructive/restrictive) pattern

A

obstructive

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116
Q

CF often chronically infected with ________ in the lungs

A

pseudomonas

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117
Q

CF treatments

A 
pancreatic enzyme replacement
fat soluble vitamin supplement
chest PT
flu and pneumococcus vaccines
tx infections with abx
inhaled rhDNase
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118
Q

2 broad categories of lung cancers and how common is each

A

small cell- 25%

non small cell- 75%

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119
Q

risk factors for lung cancer (4)

A

smoking
asbestos
radon
COPD

120
Q

which lung cancer has the least association with smoking

A

adenocarcinoma

121
Q

staging system of NSCLC

A

TNM staging

122
Q

staging system of SCLC

A

limited- just chest and supraclavicular nodes

extensive- outside chest and surpaclavicular nodes

123
Q

local manifestations (cough, hemoptysis, obstruction, wheezing) most common with what type of lung cancer

A

squamous cell carcinoma

124
Q

facial fullness, facial and arm edema, JVD, dilated veins over anterior chest, arms and face
what is it and what is it sometimes associated with

A

SVC syndrome

associated with SCLC

125
Q

hemidiaphragmatic paralysis in lung cancer pt

A

phrenic nerve palsy

126
Q

hoarseness in lung cancer pt

A

recurrent laryngeal nerve palsy

127
Q

unilateral facial anhidrosis, ptosis, miosis

A

Horner’s syndrome

128
Q

shoulder pain radiating down the arm, upper extremity weakness, Horner’s syndrome sometimes
what is this and what is it usually due to?

A

pancoast’s tumor

usually due to squamous cell

129
Q

lung cancer: malignant pleural effusion = ___________ in terms of prognosis

A

distant mets

130
Q

most common sites for lung cancer to met to

A

brain, bone, adrenal, liver

131
Q

lung cancer: SIADH assoc with ________

A

SCLC

132
Q

lung cancer: ectopic ACTH secretion assoc with

A

SCLC

133
Q

lung cancer: PTH like hormone secretion assoc with

A

squamous cell

134
Q

lung cancer: hypertrophic pulmonary osteoarthropathy assoc with

A

adenocarcinoma and squamous cell

135
Q

lung cancer: Eaton Lambert syndrome assoc with

A

SCLC

-proximal muscle weakness/fatigability, diminished DTRs, paresthesias (more common in lower extremity)

136
Q

workup for lung cancer

A

CXR
CT
tissue biopsy

137
Q

lung cancer dx: what is an important dx test but should not be used as a screening test

A

CXR

138
Q

lung cancer: what imaging is good for staging

A

chest CT with contrast

139
Q

lung cancer: what tests are good for dxing central lesions

A

sputum cytology

bronchoscopy

140
Q

lung cancer: what test can identify pts with advanced dz who would not benefit from surgical resection

A

mediastinoscopy

141
Q

lung cancer: what can be used to dx peripheral lesions

A

transthoracic needle biopsy

142
Q

pathologic confirmation is needed for dx of lung cancer (t/f)

A

T

143
Q

lung cancer: what should you do for intrathoracic lymphadenopathy?

A

biopsy

144
Q

tx for NSCLC:

what is the best option? what do you use as adjunct therapy?

A

surgery is the best option- not possible for pts with mets
use XRT as adjunct
chemo is debatable

145
Q

tx for SCLC for:
limited dz
extensive dz

A

limited dz- chemo and XRT

extensive dz- chemo only –> if they respond, then add on XRT to decrease brain mets and prolong survival

146
Q

most asymptomatic lung masses are benign (t/f)

A

T

147
Q

solitary pulmonary nodule: high risk features for malignancy

A 
age > 50
smoking
size > 2 cm
irregular borders
eccentric asymmetric clacification
enlarging
148
Q

solitary pulmonary nodules… what to do with the following

  • low probability nodules
  • intermediate probability nodules 1 cm
  • high probability nodule
A
  • serial CT scans
  • serial CT scans
  • PET –> if positive, excision
  • excision
149
Q

lung nodules with no growth in 2 years are usually benign (t/f)

A

T

150
Q

locations of lung cancers

  • squamous
  • adeno
  • large cell
  • small cell
A
  • usually central
  • often peripheral
  • usually peripheral
  • central
151
Q

most common cause of mediastinal mass in older person

A

metastatic cancer, esp from lung cancer

152
Q

common mediastinal masses by location
anterior
middle
posterior

A

anterior– thyroid, teratogenic tumors, thymoma, terrible lymphoma
middle- lung cancer, lymphoma, aneurysms, cyst, Morgagni hernia
posterior- neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek’s hernia

153
Q

clinical features of mediastinal masses usually due to ________

A

compression or invasion of adjacent structures

-cough, CP, dyspnea, pneumonia, SVC syndrome, horaseness, Horner’s, etc

154
Q

how to dx mediastinal masses

A

chest CT –> if benign looking and pt has no sxs, just observe

155
Q

criteria for exudates (context of pleural effusion)

A

pleura protein/serum protein > 0.5
pleura LDH/serum LDH > 0.6
pleura LDH > 2/3 the upper limit of normal serum LDH

156
Q

most common cause of pleural effusion + other causes

A

CHF

other causes: pneumonia (bacterial), malignancy (lung, breast, lymphoma), PE, viral diseases, cirrhosis with ascites

157
Q

signs of pleural effusion

A

dullness to percussion
decreased BS over the effusion
decreased tactile fremitus

158
Q

elevated pleural fluid amylase… think these 3 things

A

esophageal rupture
pancreatitis
malignancy

159
Q

milk opalescent pleural fluid

A

chylothorax

160
Q

purulent pleural fluid

A

empyema

161
Q

blood in the pleural space

A

malignancy

162
Q

exudative pleural effusion that’s primarily lymphocytic

A

TB

163
Q

pH < 7.2 for the pleural effusion

A

parapneumonic effusion or empyema

164
Q

if pleural fluid glucose < 60, rule out ________

low glucose in pleural fluid can be assoc with (4 things)

A

r/o RA

could be TB, esophageal rupture, malignancy, lupus

165
Q

3 ways to dx pleural effusion

A 
CXR- need 250 mL to visualize; lateral decubitus films are best
CT- more reliable than CXR
thoracentesis- good for dx and symptomatic relief 
	the 4 C's: chemistry (glucose, protein)
			cytology 
			cell count (CBC with diff)
			culture 
	complication is ptx
166
Q

tx of transudative pleural effusions

A

diuretics, Na restriction

thoracentesis only if it’s massive and causing SOB

167
Q

tx of exudative pleural effusions

A

tx underlying dz

168
Q

tx of parapneumonic effusions

A

uncomplicated- abx

complicated- chest tube, intrapleural injection of streptokinase, surgical lysis of adhesions

169
Q

parapneumonic effusion vs. empyema

A
  • parapneumonic effusion = noninfected pleural effusion secondary to bacterial pneumonia
  • empyema = complicated parapneumonic effusion (infected)
170
Q

empyema usually occurs as complication of ___________

A

bacterial pneumonia

171
Q

how to dx empyema

A

CXR and CT

172
Q

how to tx empyema

A

abx, aggressive drainage of pleura vis thoracentesis

-if severe and persistent, rib resection and open drainage

173
Q

always get a CXR after these 3 procedures to make sure you didn’t create a ptx

A

central line placement
thoracentesis
transthoracic needle aspiration

174
Q

2 categories of spontaneous ptx and characteristics of each

A

primary/simple- no lung dz, young tall lean men, severe respiratory distress usually not present

secondary/complicated- underlying lung dz (esp COPD), more life threatening due to lack of pulmonary reserve

175
Q

recurrence rate of spontaneous ptx

A

high- 50% in 2 years

176
Q

_________ hastens the resorption of air in pleural space and is first tx for spontaneous ptx

A

supp O2

177
Q

how to tx primary spontaneous ptx

A
  • if small and no sxs –> observation (resolve in 10 days) or small chest tube
  • if large and/or there are sxs –> give O2 and insert chest tube
178
Q

how to tx secondary spontaneous ptx

A

chest tube

179
Q

malignant mesotheliomas assoc with __________

common presentation includes:

A

asbestos

-SOB, weight loss, cough, bloody effusion

180
Q

drugs that cause interstitial lung disease (name 5 of many)

A 
amiodarone
nitrofurantoin
bleomycin
phenytoin
illicit drugs
181
Q

if interstitial lung disease is suspected, ask about _____ and _____

A

meds and jobs/exposures

182
Q

signs of ILD

A

rales at the bases
digital clubbing
pulmonary HTN and cyanosis in advanced dz

183
Q

what is an endstage finding of many ILDs

A

honeycomb lung

184
Q 
dxing ILD
\_\_\_\_\_\_ is nonspecific
\_\_\_\_\_\_ is very good at showing fibrosis 
\_\_\_\_\_\_ is controversial
others (3)
A

CXR is nonspecific
CT good for showing fibrosis
bronchoalveolar lavage controversial
tissue biopsy often required for pts with ILD
PFTs show a restrictive pattern (see other flashcard for PFT findings)
U/A to look for glomerular injury

185
Q

PFT findings in ILD

A

restrictive pattern

  • increased FEV1/FVC
  • all lung volumes are low
  • FEV1 and FVC are low, but the latter more so
  • low DLCO (diffusing capacity)
186
Q

if someone has digital clubbing, get _______

A

a CXR b/c chronic hypoxemia is the underlying cause in most cases

187
Q

young pt with constitutional sxs, respiratory complaints, erythema nodosum, blurred vision, bilateral hilar LAD

A

sarcoidosis

188
Q

chronic systemic granulomatous dz characterized by noncaseating granulomas

A

sarcoidosis

189
Q

sarcoidosis- typical demographic

A

AA women

190
Q

most common cause of death in sarcoidosis

A

cardiac disease

191
Q

dx of sarcoidosis is based on ______, _______, and _______ findings

A

clinical, radiographic, histologic (must see noncaseating granulomas)

192
Q

CXR in sarcoidosis pt:

__________ is the hallmark of disease

A

bilateral hilar LAD

193
Q

other findings in sarcoidosis

A

skin anergy
ACE elevated in serum
hypercalcemia and hypercalciuria

194
Q

staging of sarcoidosis (on CXR)

A
  • stage I: bilateral hilar LAD
  • stage II: bilateral hilar LAD + parenchymal infiltrates
  • stage III: diffuse parenchymal infiltrates w/o hilar LAD
  • stage IV: pulmonary fibrosis with honeycombing and fibrocystic parenchymal changes
195
Q

least favorable sarcoidosis stage

A

III

196
Q

how to tx sarcoidosis

A
  • most resolve spontaneously so no tx
  • if pts have sxs, then systemic CS
  • if refractory to CS, then methotrexate
197
Q

chronic interstitial pneumonia caused by abnormal prolif of histiocytes (related to Langerhan’s cells in the skin)

A

histiocytosis X

198
Q

presentation, dx, and tx of histiocytosis x

A
  • cigarette smokers with dyspnea and nonproductive cough +/- spontaneous ptx, lytic bone lesions, DI
  • CXR shows honeycombing, CT shows cystic lesions
  • variable prognosis
  • tx with CS (sometimes effective) and lung transplant (may be necessary)
199
Q

necrotizing granulomatous vasculitis in the kidneys, lungs, and upper airway

A

Wegener’s granulomatosis

200
Q

presentation, dx, and tx of Wegener’s granulomatosis

A
  • upper and lower respiratory infections, glomerulonephritis, pulmonary nodules
  • dx gold standard is tissue bx, + for c-ANCA
  • tx with immunosuppressants and glucocorticoids
201
Q

granulomatous vasculitis in patients with asthma

A

churg-strauss syndrome

202
Q

presentation, dx, and tx of churg-strauss syndrome

A
  • pulmonary infiltrates, rash, eosinophilia
  • skin, muscle, and nerve lesions
  • dx: blood eosinophilia, p-ANCA
  • tx: systemic glucocorticoids
203
Q

c-ANCA assoc with

p-ANCA assoc with

A

Wegener’s granulomatosis

Churg-Strauss syndrome, sometimes Goodpasture’s syndrome

204
Q

most simple coal worker’s pneumoconiosis need no treatment (t/f)

A

T

205
Q

complicated coal worker’s pneumoconiosis is characterized by _________

A

fibrosis

206
Q

asbestosis has predilection for ____________ of the lung

A

lower lobes

207
Q

asbestosis puts you at increased risk for ______ and _______

A

bronchogenic carcinoma and malignant mesothelioma

208
Q

classic CXR findings in the following:

  • asbestosis
  • silicosis
A

pleural plaques

“egg shell” calcifications

209
Q

silicosis: localized and nodular peribronchial fibrosis (______ lobes more common)
- increased risk of _______

A

upper

TB

210
Q

berylliosis has both _____ and ______forms

  • chronic dz very similar to _________ (granulomas, skin lesions, hypercalcemia)
  • dx with _____
  • tx with _________
A

acute and chronic
sarcoidosis
beryllium lymphocyte proliferation test
glucocorticoid therapy

211
Q

serum IgG and IgA to te inhaled antigen
acute form has flu like features and CXR shows pulm infiltrates
chronic form more insidious
what is it and how to tx?

A

hypersensitivity pneumonitis

tx by removing offending agent and sometimes glucocorticoids

212
Q

fever and peripheral eosinophilia
peripheral pulmonary infiltrates
what is it and how to tx?

A

eosinophilic pneumonia

tx with glucocorticoids

213
Q

IgG antibodies against glomerular and alveolar basement membranes
-hemorrhagic pneumonitis and glomerulonephritis
-presents with dyspnea and hemoptysis
what is it, how to dx, and how to tx?

A

goodpasture’s syndrome

  • dx with tissue biopsy, anti-GBM antibodies
  • tx with plasmapheresis, cyclophosphamide, and corticosteroids
214
Q

accumulation of surfactant-like protein and phospholipids in the alveoli. what dz is this?

A

pulmonary alveolar proteinosis

215
Q 
pulmonary alveolar proteinosis
CXR findings
dx
tx
what not to give
A
  • ground glass appearnace with b/l alveolar infiltrates that resemble a bat shape
  • dx: lung bx
  • tx: lung lavage, newer is granulocyte-colony-stimulating factor
  • DON’T GIVE STEROIDS
216
Q

IPF is more common in _____ and _______

  • definitive dx is _______
  • no effective tx but these may help (3 things)
A

men and smoker
open lung biopsy
O2, corticosteroids w/ or w/o cyclophosphamide, lung transplant

217
Q

cryptogenic organizing pneumonia

  • most cases are caused by __________
  • CXR and clinical findings
  • tx with _______, not ________
A

idiopathic
cough, dyspnea, flu-like sxs, bilateral patchy infiltrates
corticosteroids, NOT abx

218
Q

radiation pneumonitis

  • active form (______ after radiation)
  • chronic form (______ after radiation)
  • dx with __________
  • tx with ________
A
  • 1-6 months
  • 1-2 years
  • CT scan: diffuse infiltrates, ground glass, patchy/homogenous consolidation, pleural/pericardial effusion
  • CS
219
Q

severe hypercapnea can cause what important and terrible thing

A

increased ICP via vasodilation

220
Q

criteria defining acute respiratory failure

A

hypoxia (PaO2 < 60 and PaCO2 > 50)

hypercapnia (PCO2 > 50)

221
Q

2 major classes of acute respiratory failure

A

-hypoxemic respiratory failure- low PaO2 with a low or normal PaCO2
-caused by lung disease, often V/Q mismatch and
intrapulmonary shunt
-hypercarbic respiratory failure- decrease in minute ventilation or increase in physiologic dead space leads to CO2 retention and then hypoxia
-caused by lung disease and by NM dz, CNS depression,
mechanical restriction of lung inflation, etc.

222
Q

V/Q mismatch causes ________ without ________ and is/is not responsive to supplemental oxygen

A

hypoxia without hypercapnia

responsive to supplemental oxygen

223
Q

hypoxia due to shunt is/is not responsive to supplemental oxygen

A

is NOT

224
Q

hypoventilation causes ______ with secondary ________

A

hypercapnia with secondary hypoxemia

225
Q

diffusion impairment causes _______ w/o _______

A

hypoxemia w/o hypercapnia

226
Q

what tests to get in acute respiratory failure

A

ABG
CXR or CT
CBC and BMP
+/- cardiac enzymes if concerned about cardiogenic pulm edema

227
Q

list 3 causes of hypoxemia

A

V/Q mismatch
intrapulmonary shunting
hypoventilation

228
Q

why not give lots of O2 to chronic COPDers

A

hypoxia drives their breathing

if you give them oxygen, they hypoventilate and hypercapnia worsens causing a respiratory acidosis

229
Q

BIPAP and CPAP are meant to ______________

A

attempt to avoid intubation and ventilation in patients with impending respiratory failure
-best for hypercarbic respiratory failure (COPD)

230
Q
  • diffuse inflammatory process involving both lungs

- involves neutrophil activation

A

ARDS

231
Q

key pathophys event in ARDS:

other findings:

A
  • key pathophys event: intrapulm shunting leads to severe hypoxemia with no improvement on 100% oxygen
  • interstitial edema and alveolar collapse –> stiff lungs, increased A-a gradient, decreased compliance, increased dead space (destruction of pulmonary capillary bed), low VC and FRC
232
Q

common causes of ARDS

A 
sepsis
aspiration of gastric contents
severe trauma, fractures, pancreatitis, massive transfusion
drug OD
intracranial HTN
cardiopulmonary bypass
233
Q

criteria to dx ARDS

A
  • hypoxemia refractory to O2 therapy: PaO2/fiO2 < 200
  • b/l diffuse pulmonary infiltrates on CXR
  • no evidence of CHF: PCWP < 18
234
Q

diagnostic tests for ARDS

A

CXR
ABG- hypoxemia and respiratory alkalosis then acidosis
pulmonary artery catheter
bronchoscopy if infection is suspected

235
Q

how to tx ARDS

A

PEEP- keep O2 sat > 90%
avoid volume overload
tx underlying cause
feed them

236
Q

2 goals of mechanical ventilation in respiratory failure

A

maintain alveolar ventilation

correct hypoxemia

237
Q

when you need to be mechanically ventilated (5)

A
  • significant respiratory distress
  • impaired level of consciousness and unable to protect airway
  • metabolic acidosis w/ inadequate hyperventilation
  • respiratory muscle fatigue
  • hypoxemia (PaO2 < 70), hypercapnia (PaCO2 > 50), resp acidosis (pH < 7.2) with hypercapnia
238
Q

most common cycling method for ventilators

A

volume cycled

239
Q

initial ventilator mode in most pts with respiratory failure

  • guarantees a “backup minute ventilation that has been preset
  • pt can go over the determined rate but not under it
  • every breath “over” delivers the same predetermined tidal volume
  • all breaths delivered by ventilator
A

assisted controlled (AC) ventilation

240
Q
  • patients can breathe on their own above the mandatory rate w/o help from the ventilator (tidal volume of these extra breaths is not determined by the ventilator)
  • if no spontaneous breath, predetermined mandatory breath is delivered by the ventilator, thus guaranteeing rate
  • good for support and for weaning
A

synchronous intermittent mandatory ventilation (SIMV)

241
Q
  • positive pressure is delivered continuously by the ventilator
  • good to use to assess whether patient is ready to be extubated
A

CPAP

242
Q
  • pressure is delivered with an initiated breath to assist breathing
  • enhances respiratory efforts made by patient
  • good for weaning trials
A

pressure support ventilation (PSV)

243
Q

ET tube should be ______ above the carina

A

3-5 cm

244
Q

minute ventilation = _______ x _______

A

RR x tidal volume

245
Q

initial tidal volume:

RR:

A

8-10 mL/kg (lower is recommended for pts with ARDS and COPD)

10-12 breaths/min

246
Q

what to do with fiO2

A

initially 100% then quickly titrate down
fiO2 < 60% generally safe
if fiO2 of 0.5 doesn’t cut it, add PEEP or CPAP

247
Q

normal I:E ratio

A

1:2

248
Q

normal amount of PEEP

A

2.5-10 cm H2O

249
Q

ET tube prevents aspiration (t/f)

A

F

250
Q

perform tracheostomy when ventilator dependent for more than _____

A

2 weeks

251
Q

some complications of mechanical ventilation

A
  • anxiety, discomfort –> give benzos and opioids
  • suction tracheal secretions
  • nosocomial pneumonia
  • barotrauma
  • oxygen toxicity
  • hypotension
  • tracheomalacia
  • laryngeal damage during intubation
  • GI effects: stress ulcers, cholestasis
252
Q

definition of pulmonary hypertension

A

mean PA pressure > 25 at rest or > 30 during exercise

253
Q

how to determine cause of pulm HTN

A

CXR, PFTs, ABGs, serology, echo, cardiac cath

  • if stil not clear, get V/Q scan; either PE or primary pulm HTN (PPH)
  • PPH is a dx of exclusion
254
Q

sxs and signs of pulm HTN

A

sxs: fatigue, exertional SOB/CP/syncope
signs: loud pulmonic component of S2 and subtle lift of sternum (sign of RV dilation), signs of RV failure later on

255
Q

dx pulm HTN with 2 tests

A

ECG and echo

256
Q

pulmonary HTN in the absence of heart or lung disease

A

primary pulmonary hypertension (PPH)

257
Q

demographic and prognosis of PPH

A

young or middle aged women

poor prognosis with mean survival of 2-3 years

258
Q

common finding in PPH

A

exertional syncope

259
Q

dx of PPH

A
  • cardiac cath establishes the dx
  • CXR- enlarged central pulmonary arteries, enlarged RV, clear lung fields
  • PFTs- restrictive pattern
  • ECG- RAD and RVH
260
Q

how to tx PPH

A
  • pulmonary vasodilators- IV prostacyclins (epoprostenol) and CCBs –> perform a vasodilator trial before initiating therapy
  • warfarin (INR 2) for anticoagulation
  • lung transplant may be an option
261
Q

define cor pulmonale

A

RVH with eventual RV failure resulting from pulm HTN secondary to pulmonary disease

262
Q

cor pulmonale most commonly caused by ______

A

COPD

263
Q

signs of cor pulmonale

A 
decrease in exercise tolerance
cyanosis, clubbing
hepatomegaly, edema, JVD
parasternal lift
polycythemia if COPD is the cause of cor pulmonale
264
Q

how to tx cor pulmonale

A 
tx underlying disorder
be careful with diuretics b/c pts may be preload dependent
long term home oxygen if pt is hypoxic 
give digoxin only if LV has problems
vasodilators.... eh results
265
Q

many COPD and PE patients die from ______

A

cor pulmonale

266
Q

up to 2/3 of patients who survive PE get _________

A

pulmonary HTN

267
Q

2 studies related to PE

A

PIOPED- guides treatment if V/Q is performed

Christopher Study- guides treatment if spiral CT is performed

268
Q

most PE arise from _________

A

DVT of the lower extremities above the knee (ileofemoral)

269
Q

a very large PE could result in acute ______

A

cor pulmonale

270
Q

PE causes ______ physiology which reads to ______ and ______

A

dead space –> hypoxia and hypercarbia leading to tachypnea

271
Q

course: most often, PEs are __________
recurrences are common which lead to ____ and ________
mortality is ______ if PE is diagnosed early
_______ also reduces mortality

A

clinical silent
chronic pulm HTN and chronic cor pulmonale
decreased
anticoagulation

272
Q

if pt has sxs of PE and a DVT is found, you can dx PE w/o further testing (t/f)

A

T

273
Q

most common sxs and signs of PE

A

sxs: dyspnea, pleuritic CP, cough, hemoptysis, DVT, syncope (if very large)
signs: tachypnea, rales, tachyardia, S4, increased P2, shock (if very large)

274
Q

risk factors for DVT/PE

A 
age > 60 years
malignant
prior DVT, PE
hereditary hypercoagulable state
prolonged immobilization or bed rest
CHF
obesity
nephrotic syndrome 
major surgery
trauma
pregnancy, estrogen use
275
Q

ABG in PE

A

not diagnostic
will show hypoxemia and hypocapnia (due to hyperventilation) –> respiratory alkalosis
A-a gradient usually elevated

276
Q

CXR in PE

A

usually normal

  • mainly used to r/o alternative dxs
  • Hampton’s hump and Westermark’s sign rarely present
277
Q

venous duplex ultrasound of the lower extremities in PE

A

very useful if positive, not so useful if negative

if positive, tx with heparin regardless

278
Q

V/Q scan in PE

A

mostly replaced by helical CT now…

  • normal –> no further testing
  • high probability –> tx with heparin
  • low or intermediate probability –> clinical suspicion determines next step
    • will need pulm angiography and/or LE venous duplex
    • if duplex is positive –> tx with heparin
    • if duplex is negative –> do the angiography
279
Q

spiral CT for PE

A

decent sensitivity (85%) and good specificity (over 95%)
replaced V/Q in most places
combine with Wells criteria to guide treatment
-sxs and signs of DVT, alternative dx less likely than PE, HR > 100, immobilization, previous DVT or PE, hemoptysis, malignancy
-see pg. 108 of Step Up to Medicine

280
Q

_______ is the gold standard dx for PE

A

pulmonary angiography

  • only do it when noninvasive testing is equivocal and risk of anticoagulation is high OR
  • patient is hemo unstable and embolectomy may be required
281
Q

how to use D-dimer in PE

A

high sensitivity, low specificity
only use if low clinical suspicion
-if negative, then r/o PE
-if positive, this doesn’t help you

282
Q

workup of PE

how to definitely treat or definitely not treat people

A

need to tx:
-high probability V/Q or CT and clinical suspicion
-DVT diagnosed by ultrasound and clinical suspicion
-positive angio
no need to tx:
-low probability V/Q or negative CT and low clinical suspicion
-negative angio
-negative D-dimer and low clinical suspicion

283
Q

how to tx PE

A

-supplemental O2
-give heparin (unfractionated or LMWH) and warfarin acutely with bridge to just warfarin for 3-6 months or longer; if high clinical suspicion, don’t wait for studies before starting anticoagulation
goal PTT: 1.5-2.5 time control
goal INR: 2-3
LMWH may be better than unfractionated heparin
-thrombolysis only for pts who are hemo unstable or evidence of right heart failure
-IVC filter for ppl who can’t be anticoagulated or have failed anticoagulation or who have low pulmonary reserve and have high risk of death from PE

284
Q

aspiration pneumonia most often affects __________ and ________

A

lower segments of right upper lobe

upper segments of right lower lobe

285
Q

aspiration pneumonia develops in ______ of patients who aspirate usually _____ after aspiration. organisms are usually ________

A

40%
2-4 days
mixed (aerobic-anaerobic)

286
Q

CXR of pulmonary aspiration

A

variable
infiltrates resembling bacterial pneumonia
atelectasis and local areas of collapse

287
Q

aspiration can lead to ________ if untreated. Poor oral hygiene predisposes to such infections. Foul smelling sputum often indicates ________ infection

A

lung abscess

anaerobic infection

288
Q

if aspiration pneumonia is suspected, give _______

A

abx (penicillin G or clinda)

prophylactic abx is controversial

289
Q

if obstruction is present after aspiration of something, do this

A

bronchoscopy

290
Q

most common causes of acute dyspnea

A 
CHF exacerbation
pneumonia
bronchospasm
PE
anxiety
291
Q

tests to get for dyspnea

A

CXR
sputum gram stain and culture
PFTs ABGs
ECG, echo

292
Q

paroxysmal nocturnal dyspnea can indicate ______ and/or _______

A

CHF and/or COPD

293
Q

definition of massive hemoptysis

A

> 600 mL of blood in 24 hours

294
Q

massive hemoptysis
most common causes:
_________ is key. intubate if necessary
_________ can help identify source of bleeding
_________ to stop the bleeding if indicated

A

most common causes: bronchiectasis, bleeding diathesis
airway protection
bronchoscopy
bronchial artery embolization or balloon tamponade of the airway

295
Q

most common causes of hemoptysis in general

A 
bronchitis
lung cancer (bronchogenic carcinoma)
TB
bronchiectasis
pneumonia
others: goodpasture's, PE w/ pulm infarct, aspergilloma within cavities, mitral stenosis, hemophilia
296
Q

evaluation of hemoptysis (3 things)

A
  • CXR- may clearly show the etiology but normal CXR does not r/o a serious condition
  • bronchoscopy- do this even if CXR is normal if there is a high suspicion for lung cancer, may localize tumor and/or site of bleeding
  • CT scan- complement to bronchoscopy or substitute when bronchoscopy is contraindicated

Medicine (2 decks)

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